The disease pathogenesis of Alzheimer´s disease is associated with plaques forming from the soluble peptide amyloid-β. However, it could arise from either of two ends of the process: the increase in insoluble amyloid plaques or the depletion of the soluble peptide, which has important functions.
In this retrospective longitudinal study the hypothesis was tested, that in individuals with amyloid plaques carrying certain Alzheimer's disease-causing mutations, higher levels of soluble amyloid-β reduce the risk of cognitive progression. The cognitive function of 108 patients was quantified over 3 years, and cerebrospinal fluid biomarkers including soluble amyloid- β were determined. Neuroimaging was used to quantify the burden of insoluble brain amyloid plaques.
The results demonstrate that higher levels of soluble amyloid- β levels predict a lower risk of cognitive progression. Thus this study revealed that brain toxicity in Alzheimer's disease may be predominantly mediated by a reduction of the soluble protein pool, rather than its accrual into amyloid plaques.
High soluble amyloid-β42 predicts normal cognition in amyloid-positive individuals with Alzheimer’s disease-causing mutations
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